We demonstrate below that targeting of a potent toll‐like receptor 7 (TLR7) agonist specifically to IPF macrophages can successfully reprogram these cells, causing a significant decrease in markers of fibrosis (i.e., CCL18, hydroxyproline, and collagen), a concomitant increase in hallmarks of anti‐fibrotic activity (i.e., CXCL10, IFNα, IFNγ, and CD86) (Diaz & Jiménez, 1997; Jiang et al, 2010; Lutherer et al, 2011; Braga et al, 2015; Murray, 2017), and the anticipated expansion of alveolar airspaces. This evidence concerns the gene TLR7 and idiopathic pulmonary fibrosis.